TY - JOUR
T1 - Experimental Campylobacter jejuni infection of adult mice
AU - Blaser, M. J.
AU - Duncan, D. J.
AU - Warren, G. H.
AU - Wang, W. L.L.
N1 - Copyright:
Copyright 2020 Elsevier B.V., All rights reserved.
PY - 1983
Y1 - 1983
N2 - HA-ICR adult mice were studied to develop an animal model for Campylobacter jejuni enteritis in humans. Fecal and ileal cultures made by selective and nonselective methods showed that C. jejuni and related organisms are not bowel commensals. Intragastric feeding of 108 CFU of three different strains of C. jejuni produced infection in 100% of the animals, and infection rates were dose dependent. Pretreatment with antibiotics or opiates was not necessary to induce infection. Fresh isolates and strains passed on artificial media yielded similar infection rates. Infected mice did not show signs of illness, but transient bacteremia within 10 min of oral infection was observed in nearly 100%. The small intestine was the principal target organ, with epithelial inflammation seen 48 h after infection. Control mice of four species had undetectable serum immunoglobulin G antibody specific for the infecting strain, but infected mice showed peak titers at 1 week with rapid decline. Immunoglobulin M titers rose minimally, and immunoglobulin A titers did not rise. Infected mice uniformly became chronic asymptomatic excretors, shedding 104 to 106 CFU/g of feces; a minority were biliary carriers. Intestine carriage was most pronounced in the stomach and proximal small intestine. Because this experimental infection led to bacteremia, transient pathological changes, and immunoglobulin G titer rises, this model may be useful for evaluating the effects of prophylactic and therapeutic interventions.
AB - HA-ICR adult mice were studied to develop an animal model for Campylobacter jejuni enteritis in humans. Fecal and ileal cultures made by selective and nonselective methods showed that C. jejuni and related organisms are not bowel commensals. Intragastric feeding of 108 CFU of three different strains of C. jejuni produced infection in 100% of the animals, and infection rates were dose dependent. Pretreatment with antibiotics or opiates was not necessary to induce infection. Fresh isolates and strains passed on artificial media yielded similar infection rates. Infected mice did not show signs of illness, but transient bacteremia within 10 min of oral infection was observed in nearly 100%. The small intestine was the principal target organ, with epithelial inflammation seen 48 h after infection. Control mice of four species had undetectable serum immunoglobulin G antibody specific for the infecting strain, but infected mice showed peak titers at 1 week with rapid decline. Immunoglobulin M titers rose minimally, and immunoglobulin A titers did not rise. Infected mice uniformly became chronic asymptomatic excretors, shedding 104 to 106 CFU/g of feces; a minority were biliary carriers. Intestine carriage was most pronounced in the stomach and proximal small intestine. Because this experimental infection led to bacteremia, transient pathological changes, and immunoglobulin G titer rises, this model may be useful for evaluating the effects of prophylactic and therapeutic interventions.
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U2 - 10.1128/iai.39.2.908-916.1983
DO - 10.1128/iai.39.2.908-916.1983
M3 - Article
C2 - 6832823
AN - SCOPUS:0020681670
VL - 39
SP - 908
EP - 916
JO - Infection and Immunity
JF - Infection and Immunity
SN - 0019-9567
IS - 2
ER -